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Selenium: Its Metabolism and Relation to Exercise REVIEW Selenium: Its metabolism and relation to exercise Abdulkerim Kasim Baltaci1*, Rasim Mogulkoc1, Mustafa Akil2 and Mursel Bicer3 1Selcuk University, Selcuklu Medical School, Department of Physiology, Konya, Turkey 2Karabuk University, High School of Physical Education and Sport, Karabuk, Turkey 3 Selcuk University, High School of Physical Education and Sport, Konya, Turkey Abstract: Selenium (Se), which is commonly found in nature, is one of the essential trace elements necessary for the normal development of human and animal organisms. Selenium was first defined in 1818 by the Swedish chemist Berzelius in sulfuric acid residues. At the end of 1960s, the role of selenium in human health began to attract attention and human diseases that resembled animal diseases responding to selenium was started to be investigated. Selenium, which is highly important for human health, is necessary for a variety of metabolic processes, including thyroid hormone metabolism, protection against oxidative stress and immunity functions. Selenium is a molecule that activates glutathione peroxidase, and thus, it is involved in the antioxidant mechanisms that prevent oxidant damage. Exhaustive physical exercise is known to cause oxidant damage, probably by promoting free radical production in many tissues, including muscle, liver, heart and lungs in animals. The increase in oxidative stress during exercise and recognition of selenium’s stimulation of antioxidant activity inevitably suggest a relation between selenium and exercise. The present review aims to provide information on selenium metabolism and the relation between selenium and exercise. Keywords: Selenium, nutrition, metabolism, physical performance, exercise. Selenium binding to plasma proteins and forms a part of this tissue The major source of selenium is soil, and thus the plants. (Underwood 1977; McDowell et al., 1983). Binding to Selenium, which is transferred from soil to plants, animals the plasma proteins albumin, α1 and α2 globulins and β- and humans through the biological cycle, is consequently lipoproteins, selenium is transported to all body tissues, found in the organism in trace amounts (Oldfield, 1987; including the kidneys, liver, heart, red and white blood Shamberger 1986). Presence of vanadium, cobalt, zinc cells, pancreas tissues and hemoglobin globulin and particularly sulfates in the soil lowers the rate by (Underwood 1977; Church and Pond 1982; Mills 1970). which living things utilize selenium. The amount of Amount of selenium in the blood varies significantly selenium in arid soil is very low, causing selenium relative to its amount in the diet. Normal selenium level in deficiency in animals living on arid land (Underwood the plasma ranges between 0.08 and 0.12µg/ml. Besides, 1977). hemoglobin, myoglobin, cytochrome-C have been reported as specific proteins and aldolase and myosin Its absorption, transport and storage have been reported as specific enzymes for selenium that Selenium absorption occurs through small intestines, is transported by binding to plasma proteins, albumin in duodenum in particular, by active transport (Church and particular (Mills 1970). Pond 1982; Combs and Combs 1986; Keen and Graham 1989). Selenium as an element and selenium sulfite are Mobilization and excretion of selenium scarcely absorbed (Keen and Graham 1989; Kutsky Selenium is excreted through feces, urine and respiration. 1981). However, selenium which is taken in the organic Its rates of excretion vary according to the animal species, form through diet or converted into organic form by the its route of administration, amount of selenium per ration, organism is easier to absorb, and therefore has higher its chemical form, as well as the levels of elements like rates of absorption (Church and Pond 1982; Combs and arsenic and copper, which promote selenium excretion Combs 1986). Besides, amounts of vitamins E and A, as from the body, present in the ration (Underwood 1977). well as ascorbic acid, in the ration increases absorption of Intestinal absorption of selenium taken through oral route selenium (Combs and Combs 1986). After being ranges between 44% and 70%; 14-20% of the intake is absorbed, selenium is rapidly distributed to all bodily excreted through urine and a very small amount through organs and tissues (Keen and Graham 1989). Although skin and respiration in the first week, while 35-55% is selenium transporters have not been definitively disposed of through feces. Injections of arsenic, thallium, classified, it has been noted that it is transported by copper and cadmium increase selenium discharge by respiration, but lead and copper injections do not have any *Corresponding author: e-mail: [email protected] effect on excretion through this route (Underwood 1977). Pak. J. Pharm. Sci., Vol.29, No.5, September 2016, pp.1719-1725 1719 Selenium: Its metabolism and relation to exercise Daily selenium need and its relation to health selenium in the diet influenced functions of phagocytic Selenium in the diet usually comes from white and red cells (neutrophils, macrophages) (Boros, 1980) and that in meat, grains and bread. An adult human body contains selenium deficiency neutrophils obtained from rat, mouse 20mg selenium. Selenium which is particularly and cattle had an impairment in their ability not only to concentrated in the liver and kidney is found most phagocytize Candida albicans, but also to kill abundantly in the muscles (Levander, 1986). Amounts of phagocytized Candida albicans (Boyne at al., 1986). It daily selenium intake recommended by health was argued that lysosomal membranes of macrophages organizations are 20-30µg for children (aged 1 to 10), contained GPx and that these were destroyed in selenium 70µg for males over 20 years, 55µg for females, and 65 deficiency (Combs and Combs, 1986). Generally, µg for pregnant women (Van Campen, 1991). It was selenium deficiency produces immunosuppressive results. reported that amount of daily selenium intake in the U.S. However, supplementation of selenium at physiological ranged between 60 and 216µg and in that case, the doses has been reported to be associated with an increase amount of selenium in the blood was in the range between or improvement in the immunological response 190 and 250µg/L (Burk, 1984; Burk 1991). However, in (Kremidjian-Schumacher and Stotzky, 1987). Some New Zealand where selenium deficiency is common, experimental studies conducted on various animal species amount of daily selenium intake was reported to stand at (Dhur et al., 1990) have shown a positive correlation 28-50µg/L, in which case selenium in the blood ranged between level of selenium and resistance against between 50 and 100µg/L. In China, daily selenium intake infectious agents. It was shown that selenium-deficient was reported to be 30µg/L and the selenium in blood was animals with induced experimental infections were very 10µg/L, which is below the normal value (Van Campen, vulnerable against infections. On the other hand, cows 1991). These values indicate that there is a conspicuous and sheep supplemented with selenium were selenium deficiency in China. Selenium deficiency in demonstrated to be very resistant against infectious agents Chinese people was established to be associated with (Dhur et al., 1990). Selenium was also reported to have a basic cereal products’ containing low concentrations of positive contribution to the prevention of subclinical and selenium (Yang et al., 2010). In fact, the significance of clinical mastitis and this contribution was explained by selenium fur human health was first put forward through selenium’s possible stimulating effect on the number of Keshan disease seen in rural China. One- to 10 year-old PMN (polymorphonuclear leukocytes), immune functions children who died due to Keshan disease were found to and antibody production (Babior, 1978). have blood selenium concentrations between 8 and 26µg/L. It was noted in the same study that having blood Symptoms of selenium deficiency in domestic animals selenium concentration in the range between 32 and 83 and humans have been examined in detail. These include µg/L might bring about the risk of premature death due to degenerative disorders in many tissues, defective heart disease (Jackson 1988; Burguera et al. 1995). reproduction and growth, increased susceptibility against Burguera et al., (1995) analyzed selenium in gastric cardiovascular diseases, immune defects and some tissues of healthy individuals, as well as people with cancers (Keen and Graham, 1989). gastritis, ulcer and stomach cancer. Their results demonstrated that selenium concentration in gastric tissue It was noted that presence of 0.05-0.10µg/g and more was 473µg/L in healthy individuals, 355µg/kg in selenium was enough for protection against deficiency individuals with ulcer and 36µg/kg in individuals with syndrome in animals and that the syndrome occurred chronic gastritis. These results show that selenium has an when the amount of selenium was less than 0.05µg/g important role in preventing the development of (Oldfield, 1987; Keen and Graham, 1989). However, it cancerous tissues. Likewise, research about the relation was reported that dietary selenium concentration should between selenium and cancer revealed that physiological be in the range between 0.10 and 0.20µg/g values in order doses of selenium in humans were not carcinogenic and for optimal GPx activity to occur in tissues and that when even had an anti-carcinogenic effect (Oldfield, 1987), and dietary selenium
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